Marcelletti J F, Johnson C S, Mortensen R F, Furmanski P
J Lab Clin Med. 1982 Jul;100(1):70-80.
Pathophysiological concentrations of CRP inhibited the in vitro clonal proliferation of CFU-C's. CRP inhibition was specific for normal CFU-C's committed to the mononuclear phagocyte lineage. Macrophage progenitor cells stimulated by an inflammatory response were unaffected by CRP. CFU-C's which were committed to the granulocyte lineage, those which gave rise to both macrophages and granulocytes, and erythroid progenitor cells were also not affected by CRP. Only macrophage CFU-C's that possessed Fc receptors and were in S-phase at the time at CRP exposure were susceptible to inhibition of colony formation. The data suggest that CRP functions as a regulator of the cellular composition of an inflammatory response.
C反应蛋白（CRP）的病理生理浓度抑制了体外集落形成单位-粒细胞（CFU-C）的克隆增殖。CRP的抑制作用对单核吞噬细胞谱系的正常CFU-C具有特异性。由炎症反应刺激的巨噬细胞祖细胞不受CRP影响。定向于粒细胞谱系的CFU-C、产生巨噬细胞和粒细胞的CFU-C以及红系祖细胞也不受CRP影响。只有那些具有Fc受体且在暴露于CRP时处于S期的巨噬细胞CFU-C易受集落形成抑制。这些数据表明CRP作为炎症反应细胞组成的调节剂发挥作用。
